The role of calcium in initiating smooth muscle contraction is widely documented. The intracellular sites that have been suggested to act as calcium sources have not clearly delineated although the plasma membrane, sarcoplasmic reticulum, and mitochondria have the capacity to sequester calcium. We proposed to use 45Ca electron microscopic (EM) autoradiography (ARG) to examine the cellular distribution of calcium in smooth muscle in the presence and absence of pharmacological agonists and antagonists. From these data we can deduce the ultrastructural sites that function as calcium sinks and sources for contraction and more clearly define how spasmolytic agents modify the functional operation of these sinks and sources. By carrying out these studies in different types of smooth muscle, one can determine if different muscles utilize different cellular calcium pools. We anticipate that by studying the sources and sinks of activator calcium in vascular muscle under a variety of experimental conditions, we will more clearly understand the mechanism through which excitation-contraction coupling occurs in vascular smooth muscle.